GI Flashcards
SMA syndrome
- what happens
- sxs
- worse
- improve
- duodenum compressed by SMA
- stomach pain
- eating
- left lateral recumbent
Obstruction of duodenum
- how to fix
- re-route GI tract so food can bypass blockage
IMA
- supplies
- gives off
- distal part of transverse colon, descending, sigmoid,
- inferior rectal a
SMA
- supplies
- great colic artery
- ileocolic artery
- lower duodenum, small intestine, ascending colon, and prox 2/3 colon
- ascending colon
- ileum and cecum
What is first part of GI to be affect with hypotension
- splenic flexure, only gets some flow from IMA and SMA
marginal a of drummen
- sits against wall of intestine
arc of riolan
runs in mesentary, communicates between IMA and SMA
Blood supply to liver
- artery
- runs w
- pringle manuever: what is it, what does it mean
- triad anatomy
- venous
- proper hepatic
- portal v and bile duct
- clamp duct, a, v when there is bleed in liver -> if continue to bleed then it is venous
- ant: bile duct, artery, portal v
- right, middle, and left hepatic v -> dump into vena cava
Embryology
- starts as
- leaves
- returns
- turns
- foregut: includes, a, PS, S, lungs
- migut: includes, a, PS, S, rotation
- hindgut: includes, a, PS, S
- straight tube
- abd cavity through umbilicus at 6 weeks
- abd cavity at 10 weeks
- 270 degress counterclockwise
- esophagus, stomach, liver gall, upper duodenum -> Celiac trunk, PS- Vagus, S: splanchnic; gives rise to lung buds
- lower duodenum, small intestine, ascending colon, and prox 2/3 colon -> SMA, PS - vagus, S: splanchnic; rotation requires cilia and if have dyskinesia then will have all organs on opp side
- distal 1/3 of transverse colon, descending colon, sigmoid colon -> IMA, PS: pelvic splanchnic, S: lumbar splanchnic
- malrotation: cecum, midgut, sxs; worst case scenario; tx
- cecum is in RUQ and held in place by ladds bands; midgut fixed to SMA; newborn baby in first few days of lay has bilious vomitting; malrotation causes necrosis and gangrene of intestines; surgery -> remove bands, remove necrotic tissue -> put everything back in place (cecum will end up in LUQ, so remove appendix)
acute mesenteric ischemia
- sxs
- palpation
- pt in excutiating pain but do not see much on PE, signs of sepsis
- doughy on palpation
Anus
- upper: contains, mucosa histo, connects to lower w, blood supply
- lower: histo, blood supply
- hiltons white line: what is it
- dentate line: what is it and why is it important
- longitudinal folds/ elevations of mucosa; simple columnar epi; connectes w/ anal valves; sup rectal
- stratified squamous epi; inferior rectal
- junction between keratinized stratified squamous epithelium and non-keratinized stratified squamous epi
- above is rectum w/ columnar epi (colorectal CA) and visceral innervation (painless); anus w/ squamous epi (squmous cell CA) and painful
Retroperitoneal stuctures
- solid
- hollow
- vessels
- SAD pucker
- cause of retroperitoneal hematoma in stable pt
- pancreas, kidney, adrenal
- part 2-3 of duodenum, ascending and descending colon, rectum, ureters, bladder
- abd aorta, inferior vena cava
- pancreatic injury w/ venous bleeding
Tongue
- taste
- Pain
- motor
- ant 2/3 tongue
- post 1/3 tongue
- taste
- 7, 9, 10
- 3, 9, 10
- 12
- 1st branchial arch; tast from chorda tympani of CN7, sensation from madibular division of 5
- 3rd and 4th branchial arches; tase and sensation from CN 9
- inside taste bud is gustatory cell which has gustatory hair which detects chemical compound you are injesting, activate sensory fibers and they take info to brain
Oral gland innervation
- PS
- Symp
- parotid
- lingual
- sublingual
- submandibular
- increase secretion
- decrease secretion
- serous -> CN9
serous -> CN7 - mucinous -> CN7; under tongue
- mucinous -> CN7; under jaw
Saliva
- 1st step in
- rich in
- lipase
- amylase
- lysozyme
- HCO3
- digestive process
- IgA
- break down fat
- begins carb breakdown; bacteria in mouth break down carb -> produce lactic acid -> destroy enamel -> lead to dental carries
- detergent that binds and reoves things from teeth that get stuck near mucinous secreting glands
- protect teeth and gum from acid erosion from food, frinks, and reflux
Cleft lip
- what is it
- when does it develop
- what happens
- caused by
- failure of fusion of maxillary and medial nasal process
- week 5
- under dev of of mesenchyme of maxillary swelling causing inadequate contact w/ medial nasal process and intermax process
- anti-seizure, vit A
Cleft palate
- develops
- caused by
- tx
- 8 weeks - 12 weeks
- lat palantine process, nasal septum and/ or median palantine process
- in US fixed immediately but in other countries w/o resources will have to wait till older sometimes even adult hood
Swallowing
- process
- chew food and mix with saliva to form paste -> tongue pushes bolus into post oral pharynx -> soft palate elevates to close nasopharynx -> larynx blocks trachea so you dont aspirate -> bolus goes down esophagus
Muscles of tongue
- mylohyoid
- genioglossi
- styloglossus
- hyoglossus
- palatoglossus
- tongue elevation
- tongue protrusion
- trough formation
- tongue depression and retraction
- elevates post tongue and closes oropharyngeal isthmus; innervated by vagus
Odynophagia
- what is it
- bugs
- healthy person causes
- painful swallowing
- candida or CMV (cowdry bodies)
- pill swallowing
Dysphagia
- what is it
- progressive worsening
- chronic
- paradoxical
- cardiovascular
- difficulty swallowing
- stop solids first, then soft food, then liquids; cancer
- achalasia ->
- only with liquid
- dilated left atrium pushing on esophagus; will have mumur and rales with pain
Dysphagia
- what is it
- progressive worsening
- chronic
- paradoxical
- cardiovascular
- difficulty swallowing
- stop solids first, then soft food, then liquids; cancer
- achalasia -> LES fails to open up during swallowing
- only with liquid
- dilated left atrium pushing on esophagus; will have mumur and rales with pain
Achalasia
- what happens
- caused by
- bug
- dysphagia types
- barium swallow
- increased risk of
- mgmnt
- LES fails to open up during swallowing
- auerbach/ myenteris plexus -> unopposed PS causing contraction of LES
- chagas dx -> destroys myenteric plexus
- chronic and paradoxical
- bird beak
- esophageal CA
- Ca channel blocker and Nitrates -> SM relax (GERD), botox which causes paralysis of muscle 4-6 months of relief, mechanical dilation
Barrets Esophagus
- what is it
- caused by
- common cause
- management
- metaplasia of squamous epi to columnar epi
- chronic gastric acid exposure
- hiatal hernia -> increase in GERD (only 6% chance)
- should be scoped and biopsied every year to monitor for CA
CA of esophagus
- squamous: risk, location
- adeno: common,risk, location
- sxs
- smoking and EtOH, prox; flattened polyhedral or ovoid elpi with eosinophilic cytoplasm, keratin pearls of whirls; esophageal resection (either pull stomach into chest to attach or take part of colon and put it as a link between stomach and esophagus
- most common; barrets, distal;
- weight loss, dysphagia
Mallory Weiss tear
- what is it
- caused by
- bleeding time
- sxs
- diff from varices
- longitudinal tear of mucosa at gastro-esoph junction
- reching, coughing, vomitting
- EtOH use of eating disorder
- stop abruptly in 24-48 hrs
- blood in mouth or melena
- will vomit bucket of bloods vs only a bit of blood
boerhaave syndrome:
- what is it,
- hammans sign ,
- pleural fluid tap;
- tx
- esophageal rupture,
- usually iatrogenic,
- crunch in precordium that is synchronous with heartbeat;
- amylase, lipase, w/ contents from saliva
- drain and resect/ or tie off and give them a feeding tube directly into stomach
zenkers diverticulum
- what is it
- caused by
- sxs
- sequeleae
- diff from traction
- false diverticulum that sits about UES
- congenital or excessive pressure (problem with synchronized contraction, upper and lower muscles squeeze at same time causing increase and pressure and an outpuching)
- dysphagia, halitosis (food get stuck in out pouching), or asymptomatic
- problem with synchronized contraction -> peristalsis
- inflamm process causes adhesion and the diverticulum is caused by pulling and is true vs zenckers is pushed out bc of pressure and it is false
Plummer vinson syndrome
- triad of findings
- location
- increase risk of
- management
- dyphagia (to solids), esophageal webs, iron def anemia
- proximal
- squamous cell CA
- teat anemia, modify diet to make pt comfortable, only resect rings w/ severe odynophagia
Schatzki ring
- location
- sxs
- management
- web in lower esophagus
- intermittent dysphagia, and felling of food sticking when swallowing
- modify diet
Diffuse esophageal spasm
- what is it
- sxs
- triggered
- imaging
- tx
- uncoordinated contraction of whole esophageal body (LES remains intact)
- dysphagia, regurg, severe CP (mimics MI)
- very hot or cold beverages
- corkscrew
- CCB, nitate -> relax muscles, botox or surgical balloon dilation
tracheo-esophageal ridges
- when
- sxs
- imaging
- H configuration
- type C
- failure of fusion of tracheoesophageal ridges during 3rd week of embryogenesis
- on very first feeding baby will vommit of choke
- see blind pouch and air in stomach if trachea is attached to stomach
- esophagus attached to stomach and trachea; no vomitting but every feed child will aspirate
- most common; prox esophagus ends in blind pouch and lower is attached to stomach and trachea
GERD
- what is it
- associated w
- sxs
- increased risk of
- DX
- abnormal relax of LES allows stomach contents/acids to move into lower esophagus
- hiatal hernia
- heart burn, cough (if acid comes into pharynx), erosion of dental enamel, laryngitis, pharyngitis
- barrets
- pH probe, also known as esophageal manometry
Esophageal Varices
- what is it
- MCC
- route
- dx
- tx
- overly dilated v in lower esophagus
- portal HTN secondary to cirrhosis
- Portal vein -> left gastric v -> superficial esophageal v
- endoscopy
- ligate, band or inject them if not bleeding and cauterize or tamponade (with balloon) if bleeding
Anatomy of Stomach
- orad: where,
- caudal: where
- middle of body and up; much thinner muscular wall than distal part; higher risk of perforation
- middle of body and down; rugae are larger and thicker musclar walls; churning
Function of Stomach
- protein digestion
- vit B 12
- gastric resevoir
- occurs mainly in stomach via parietal cells producing HCL and chief cells producing pepsinogen (converted to pepsin with low pH)
- parietal cells secrete intrinsic factor to allow absorption in terminal ileum; with gastrectomy will have lifelong B12 supplementation
- holds food while partitions small amounts to go through small intestine so digestion can occur properly
Acid secretion
- celiac phase: mediated by; triggered by
- gastric phase: mediated by; triggered by
- intestinal phase
- mediated by PS; thought/ site/ taste of food causes production of gastric acid
- mediated by presence of gastrin; chemical stimulus of food and distention of stomach
- when protein contains food enters duodenum
- mucous cell: prduce, in response to
- parietal
- chief
- G cells
- interchromafin cells
- D cells
- mucus and biarb bc of prostaglandin
- HCl
- pepsinogen
- gastrin
- histamine -> increase secretion of acid
- somatostatin -> inhibits secretion of acid and peristalsis
Receptive Relaxation
- what is it
- how does it work
- VIP
- allows stomach to relax in orad region to allow more room for food
- detect stretch -> send afferent through vagus to brain and efferent through vagus to stomach releasing VIP
- SM relaxation
Gastric emptying
- time frame
- why is it reg
- slows down bc
- CCK
- why acid
- 3 hour
- allow neutralization of stomach acid duodenum and optimal absorption
- Acid (myenteric plexus) and fat (CCK)
- causes gallbladder to contract so bile can enter into duodenum so fat can be broken down into smaller globules and lipase has more SA to breakdown fat
- acid must be neutralized in order to get more food into duodenum
How is acid produced
- histamine
- gastrin
- Ach
- binds H2 receptor on parietal
- produced by g cells, binds to parietal cell; also causes release of pepsinogen
- from vagus; can cut branches of vagus nerve that go to parietal cells
Dumping Syndrome
- what is it
- sequelae
- sxs
- connect duodenum to esophagus
- no longer have pylorus to partition off amount of food in stomach so now have hyper osmotic in lumen causing water to be dumped into intestine
- hypovolemia, hypoglycemia (all glucose dumped into duodenum causes lots of insulin to be released), diarrhea, flushing, bloating
Gastrinoma
- what is it
- location
- produces
- sxs
- other tests
- managment
- neuroendocrine tumors, benign lesion
- pancreas, between pancreas and duodenum, 2nd part of doudoneum
- gastrin -> no feedback -> excessive acid production
- ulcers in weird places (NOT in stomach or in 1st portion of duodenum), diarrhea,
- MEN1 (PTH)
- PPI and removal if good candidate
Protecting stomach
- what
- stimulated by
- other mech
- mucus
- prostaglandin -> from AA
- HCO3 -> neutralizes
Parietal Cells - release - location - histo -
- HCl (H/ K on apical side) and IF
body and fundus - eosinophilic sytoplasm, increased mito and internal tubulovesicular sxs
- Ach on M3, Histamine on H2, and gastrin on gastrin receptor
Tx of acid production
- antacid
- milk alkali
- H2 blockers
- PPI: MOA, benefit, AE, azole
- mostly use CaCO3
- drink milk and take a lot of antacids -> overwhelming body w/ Ca
- only drop by 70%; ranitidine, cimetidine; antisedative, gynecomastia
- stops production of acid -> 0 acid production occurs; omeprazole and pantoprazole; Ca issues bc no neg feeback from gastrin and it stimulates PTH and also decreases amount of Ca being absorbed; cannot give azole with it bc they need acidic pH to be activated
Systemic mastocytosis
- what is it
- sequelae
- prolierfastion of mast cells in BM and other organs causing deposition of nest of mast cells in mucosa
- produces histamine causing immune reaction; looks like allergic reaction -> will cause hyper-secretion of gastric acid
Zollinger Ellison syndrome
- what is it
- leads to
- when excess gastrin is secreted by tumor
- ulcers in weird area or ulcer dx that needs to be given really high dose in order to control
Erosion
- what is it
- vs ulcer
- superficial defects that do not go beyond mucosa
- defects through submucosa and can get into muscularis and through serosa to perforate
H. pylori
- damages
- tx
- types of AB
- mucous layer making acid pass through epi cells
- 2 antibiotics, anti-secretory agent (PPI or H2b blocker) and bismuth (decrease adherence to mucousal cells and damage bacterial cell wall)
- amox, carithromycin, metro, tetracycline
Diarrhea
- common causes
- osmotic
- secretory
- toxin
- viral-bacterial
- chronic
- infection, toxins, drugs
- too much in lumen causing water to be secreted to normalize - > will stop if pt stops eating
- something causing enterocyte to secrete water
- self limited
- transient but clears faster with antibiotics if bug is found
- 3 or more lose stools per day for 3- 4 weeks; lactase def, malabsorption, lax abuse, IBS
Constipation
- first thought should be
- other causes
- idiopathic tx
- drugs (pain meds, iron)
- neurogenic (SC injury, spinabifida), endocrinpathy (DM), IBS
- bulk forming lax, dietary mod, increase fluid
Gastritis
- type a
- type b
- causes
- acute caused by
- chronic: a, b, ab, chemical
- body
- antrum
- upper GI bleeds in children, teens, adults
- h. pylori, other infections
- a- AI, b- h. pylori, AB - environmental, chemical - reflux
Peptic Ulcer Dx
- gastric: location, worse, associated with (2)
- duodenal: location, improves, worsens, associated, dx
- noraml sxs
- alarming sxs: why
- antrum; with meal; H. pylori (70%, urease breath) and CA (20%)
- duodenal bulb (any other location is suspicious for zollinger-ellison); with meal (pylorus will be shut and no acid is coming into duodenum), 30-45 min after meal (allows for gastric contents to be let in) and night (bc of motilin); H. pylori (95%); urease breath test for H pylori
- epigastric pain (burning), fullness, bloating, early satiety, nocturnal pain
- anemia, hematemesis, heme in stool, bloody vomit, persistent abd pain that radiates to back, severe abd pain that spreads; ulcer has eroded
Hiatal Hernia
- what is it
- sliding: what happens, sequelae
- rolling: what happens, tx
- whole GE junction moves above diaphragm; GERD
- defect in diaphragm allows for somtach to herniate above diaphragm; surgical correction
Gastric CA
- sxs
- mets
- epi
- risk
- adeno CA: intestinal, diffuse
- lintis plastica
- dx
- tx
- prognosis
- abd upset, abd distention, anorexia, weight loss
- left supraclavicular (virchows), sister mary joseph nodule (umbilical), krukenberg tumor (ovary)
- men over 50
- high in salt and fat and low in fiber
- solid mass that projects into lumen and is glandular columnar or cuboidal cells; infiltrates stomach wall and displays signet ring patter (cells that dont form glands)
- leather bottle stomach, diffuse infiltrating CA that is rapidly fatal
- biopsy
- palliative
- 5% for 5 yr survival
Inguinal Hernia
- epi
- presentation
- tx
- direct
- indirect
male
- groin mass
- surgical correction
- protrudes directly though abd wall, medial to epigastric a
- lateral to inf epigastric a and into spermatic cord
Femoral Hernia
- epi
- sxs
- tx
- reducible
- incarcarated
- strangulated
- females
- mass below inguinal ligament and on medial portion of thigh, painful
- urgent surgery
- herniated tissue put back in normal location
- herniated tissue not reducible menually
- vascular supply is compromised and is ischemic
Umbilical Hernia
- caused by, sxs, tx
- epi
- adult equivalent: what is it, tx
- congenital malformation; pt has outtie belly button; usually reduces on own
- AA
- paraumbilical, on one side or other instead of midline; surgical repair
Menetrier dx
- what is it
- parietal cell sequelae
- sxs
- associated with
- tx
- hyperplasia of goblet cells and enlarged rugal folds -> excessive mucus production and protein loss
- cells atophy -> decreased acid production
- weight loss, n/v, edema (loss of oncotic pressure)
- CMV and h pylori
- cetuximab (mab against EGFR) or
Pyloric stenosis
- what is it
- when is it seen
- sxs
- why
- PE
- pyloris hypertrophied and blocks outflow of stomach
- 3rd-4th week of life
- projectile vomiting
- stomach has been stretched out from being filled up with past feedings and causes reverse
- olive sign at epigastrum or to side of epi
- correct fluid and electrolytes then to surgery
Duodenal hormones
- I cells: produce, which does
- G cells
- D cells
- Pasarsym ganglia
- small intestine
- S cells
- K cells
- CCK; increase GB contration, pancreatic secretion
- produce gastrin; increase gastric acid secretion; release pepsinogen and acid
- somatostatin; slow down GI motility and secretion
- VIP; SM relaxation, and increase secretion of water and electrolytes in intestine
- motilin; propels GI
- secretin; increase bile and pancreating HCO3 secretion; acid/fat in duodenum
- GIP; increase insulin release and decrease gastric acid secretion
Structure of small intestine
- serosa
- muscularis externa
- submucosa
- peyers patches
- goblet cells
- paneth cells
- in ileum, jejunum, and 1st part of duodenum; 2nd-4th is adventitia (wet tissue paper consistenct, not able to hold stitches)
- deep to serose, has inner circular and outter longitudinal layer
- contain brunners glands (produce alkaline fluid) in duodenum and meissner plexus throughout
- only in ileum
- throughout but increase from prox to distal
- maintain intestinal epi and replenish epithelial cells
Duodenal Course
- 1st part
- 2nd part
- 3rd
- 4th
- duodenal bulb, only part introperitoneal, oriented horizontally
- goes inferior from L1-L3, location of bile duct
- horizontal over L3, abd aort and IVC; can get trapped under SMA
- sourses superior and to left of L2/3 vert and becomes jejunum when it passes ligament of treitz
Digestion of small intestine
- where do enzymes come from
- activated by
- enterokinase def: sxs, tx
- lipid digestion vs absorption
- pancreas
- trypsin, comes from trypsinogen in pancreas, converted by enterokinase
- diarrhea, malabsorption, etc; pancrease (pancreatic enzymes in pill form)
- duodenum vs jejunum; dont need transporter, just diffuse through brush border and then inside are put into chylomicrons to be transported
Peristalsis
- under control of
- include
- start -> end
- hurschprung dx: presentation, imaging, diagnosis, tx
- PS
- meissner and auerback plexi
- 8th week - 12th week
- aganglionosis of rectum; abd distention, no meconium, obstruction; dilation of colon that is atophic; rectal biopsy showing aganglionosis; colostomy bag so baby can evacuate stool, then when older the innervated part sewn down to anus and un-innervated part removed
IBD
- crohns vs UC
- signs and sxs
- dx
- affects small intestine but is seen from mouth to anus and has skip lesions; UC only involves large intestine and is continuous
- abd pain, diarrhea, malabsorption, fever
- colonoscopy + biopsy (non-caseating granuloma w/ cobblestone mucosa)
- sulfasalazine, steroid, immunosuppressive agents
Small bowel obstruction
- caused by
- sxs
- dx
- tx: small
- tx: severe/ septic
- adhesion (scar tissue from previous operation), CA, hernia, inflammation, gallstones, drugs (narcotic and anti-cholinergic)
- abd pain (crampy, in waves) and distention, tympany, high pitched bowel sound (sounds like glasses clinking together), n/v, lack of flatus
- xray: w/ mult loops of distended loops of small bowel and upright air fluid level
- conservative- NPO, NG tube and suck everything out, morphine for pain, saline to keep hydrated
- surgery required but need to give antibiotics
Small Bowel CA
- sxs
- dx
- types
- tx
- abd pain, weight loss, anemia, vomiting, obstruction
- biopsy
- adenocarcinoma, carcinoid, lymphoma and sarcoma
- resection + LN biopsy
Pancreatic embryo
- dorsal pancreatic bud
- ventral pancreatic bud
- fuse
- annular pancreas: what is it, sxs
- pancreatil tailm body, isthmus, accessory duct
- head, uncinate
- at 8 weeks
- central pancreatic bud cleaves into 2 parts and forms ring around descending portion of duodnenum an fuses with dorsal bud on each side, duodenal stenosis w/ recurrent bilious vommitting
Pancreas
- endocrine function
- exocrine function
- insulin (beta) and glucagon (alpha), somatostain (delta)
- pancreatic enzymes secreted by acinar cells into descending oart of duodenum
Pancreatic Enzymes
- amylase
- lipase: function, level, orlistat
- breaks 1,4 glucosidic bond
- ## hydrolyze dietary fat turning them into monoglycerides and FFA; normally low and if elevated can indicate acute pancreatitis; inhibits pancreatic lipase enzyme leading to decreased abiltiy to breakdown and absorb fat
Pancreatitis
- what is it
- sxs
- cause by in children
- caused by in adults
- dx
- mgmnt
- ransons criteria
- psudocyst: what is it, sxs, DX, TX
- acute interstitial: pathogenesis
- acute necrotic pancreatitis
- hemmorhagic pancreatitis: what is it; grey turner sign; cullen sign, dx
- inflammation of pancreas
- mid-epigastric pain that radiates to back
- abd trauma, infections
- alcohol, gallstones
- serum lipase and amylase, abd xray
- NPO, NG tube, IV NS, opioid,
- help predict prognosis of pancreatitis; if 3 or more met, then its severe
- pseduocyst -> collection of pancreatic enzymes, necrotic debris, and hemolyzed blood; mult bouts of pancreatitis mimicking sxs; US; drain w/ sxs
- obstruction -> stasis of pancreatic secretion -> digestion of adipose cells by lipase -> FA bind to Ca and precipitate insoluble Ca salts -> area of focal necrosis and Ca induce inflammatory reaction -> pancreas edematous
- inflammation continues -> blood flow slows -> ischemia damages acinar cells -> abnormal intracellular activation of trypsin -> other enzymes activated -> autodigestion; destruction of blood vessels and cause hemmorrhage into necrotic area (looks like chalky fat necrosis)
- bleeding into retroperitoneal space; flank bruising, periumilical bruising; CT
Pancreatic CA
- presents w
- risks
- painless jaundice, palpable non-tender gallbladder, weight loss, dark urin, pale stool
- 65-75 yrs, smoking, diabetes, chronic pancreatitis, genetics
D-xylose test
- function
- results
- test brush border absorption capabilities
- if microvilli are working then there will be high levels in urine and if not working there will be low levels in urine
Zones of liver
- zone 1: blood flow, function, affected by
- zone 2
- zone 3: blood flow, function, affected by
- oxygenated near portal triad; gluconeogenesis, beta oxidation, chol synthesis, glycogen synthesis from lactate, urea cycle; affected by toxins
- can become zone 1 if necessary; bridging necrosis from hepatitis
- least oxygenated near central vein; triglyceride synthesis, ketogenesis, glycogen synthesis from glucose, glycolysis, lipogenesis, cytochrome p450 detox; ischemia
Steatosis
- micro: what are they, nucleus,
- macro: how often, caused by, when does it become problem
- small intra cytoplasmic fat vacuoles that accumulate in cell, do not displace nucleus; reye syndrome, acetminophen tox, pregnany
- more common; alcoholic obesity; increased FA w/ problem with triglyceride synthesis or elimination; benign until inflammation occurs
- alcoholic steatosis, alcoholic hepatitic, cirrhosis
Gallbladder problems
- cholelithiasis: what is it, sxs, risk factors, dx, meds, tx, pregnant
- acute calculous cholecysittis: what is it,
- cholecystitis: what is it, bugs, sxs, labs, emphesematous
- calcified gallbladder; RUQ cramping pain + normal alk phos -> stone in cystic duct OR RUQ pain + elevated alk phos -> stone in common bile duct; female, forty, fertile, fat; US then HIDA; ursodeoxycholic acid -> breaks up stone; chole, chole during 2nd trimester
- stone has obstructed in neck of gallbladder or in cystic duct;
- inflammation of GB due to stone obstruction at GB neck or cystic duct- > disrupts GB mucus layer exposes epi to bile -> gallbladder inglamed; pressure in gallbladder builds up, causes ischemia
- infection that occurs secondary to obstruction; E. Clo, Enterobacter, Enterococcus, Klebsiella (come from intestine bc of inflammation); severe RUQ pain, murphys sign; elevated WBC w/ elevated alk-phos; caused by clostridium infection of gallbladder; cipro and metro then surgery
Pregnancy and OCP use
- estrogen: what does it do, sequelae
- progesterone: what does it do, sequelae
onfluences cholesterol syn by upregulating the activity of HMGCoA reductase enzyme -> bile become super sat with chol
- reduces bile acid secretion and slows emptying of GB -> GB is hypermotile and w/ too much cholesterol to bile salts cholesterol will precipitate out making stone
Total Parenteral Nutrition
- what is it
- prolonged causes
- how
- ileal resection: what happens, management
- all nutrition coming through IV
- can cause gallstones to form
- since not eating anything not producing CCK and so gallbladder sits static which leads to stones
- disturbs enterohepatic bile acid circulation leading to supersaturation of hepatic bile with chol, exogenous admin of CCK to keep GB from becoming too static
Gallstone Ileus
- what is it
- how does it get there
- sequelae
- sxs
- dx
- tx
- large gallstone obstructs the ileocecal valve
- through cholecyst enteric fistula
- bowel obstruction
- n/v, high pitched bowel sounds, cant pass gas
- upper GI series with air in biliary tree
- milk the stone back to jejunum, make small incision, push out, sew up, remove fistula and gallbladder
Gallbladder Hypomotility
- what is it
- caused by
- what happens
- slude contains
- associated with
- slow or icomplete GB emptying
- CCK resistance
- bile precipitation with sludge formation,
- chol monohydrate, calcium bilirubinate and mucus
- pregnancy, rapid weight loss, prolonged parenteral nutrition, spinal cord injuries
Opioids and biliary colic
- what happens
- how
- what to give instead
- can make biliary colic worse
- binds to mu receptors on sphincter of odi -> causes spasm -> increase pressure in ile duct -> increase pressure in GB -> worsen pain
- meperidine or NSAID (ketorolac -> injectable, only 5 days)
Porcelian Gallbladder
- seen in
- what happens
- sxs
- dx
- dx/tx
- pts with chronic cholecysitits, recurrent episodes over time
- bluish, brittle, calcium laden GB; scared, shrunken, Ca laden
- episodes of RUQ pain; may feel firm mass in RUQ
- HIDA
- endoscopic retrograde cholangiopancreotography; can inject dye to look at anatomy and look for patho, can also do brushing to get cells to check for CA
Choledocolithiasis
- what is it
- sxs
- dx
- tx
- stone in common bile duct -> bile cant get into dudoenum
- obstructive hjaundice, increased bili, hypercholesterolemia
- US
- chole
Ascending cholangitis
- what is it
- charcot triad
- reynolds pentad
- dx
- tx
- bile flow obstruction -> CBD obstructed -> climbing infection
- jaundice, RUQ pain, fever
- 3+ hypotension + alt mental status
- CBD dilation on US, or ERCP for definitive dx
- remove stone to decompress biliary tree
Primary sclerosing cholangitis
- type of dx
- what is it
- looks like
- sequelae
- also usually have
- epi
- AI
- inflammation and obstruction of intra and extra hepatic biliary tree
- narrowings and dilations of biliary tree -> beads on string
- bile cant get out -> cirrhosis, liver failure, CA
- IBS, ANCA, ANA
- men
Extrahepatic biliary atresia
- what is it
- sxs
- labs
- tx
- prognosis: w/o liver transplant
- congenital obstruction of extrahepatic bile duct
- juandice by 3rd-4th week life
- increase bili, alk phos, gamma glutamyl transferase
- take piece of intestine and sew to liver so that bile can drain like its supposed to; will need transplant at some point
- survival rate is 30-50%
Gallbladder CA - epi - kind - sxs - parasite - courvoisiers law -> sign -
- female with gallstone hx
- adeno
- steady RUQ pain
- chlonorchis senensis
- precense of enlarged non tender GB is more like due to CBD obstruction secondary to pancreatic CA; palpable non tender gallbladder
Primary biliary cirrhosis
- type of dx
- what happens
- gross findings
- sxs
- dx
- AI
- damages intrahepatic bile ducts -> causes liver damage
- liver is green
- pruritis (hyperbilirubinemeia), H/S megaly, xanthomas, jaundice
- anti- mito antibodies
Portal HTN
- wha is it
- pre-hepatic
- intra hepatic
- post hepatic
- sxs
- management
- side effect of management
- greater than 5 mmHg in portal v
- portal v thombosis, congenital atresia
- cirrhosis, hepatic fibrosis
- hepatic v thrombosis, IVC thrombosis, IVC congenital malformation
- ascites, splemoegaly, varices, hepatocellular encephalopathy
- TIPS: go through jugular v and into vena cava -> into the hepatic v -> take needle and go across parenchyma to get to portal v -> place stent between hepatic and portal v
- decreases ability of liver to get rid of ammonia because blood is being pumped straight back into IVC instead of being filtered in liver
Bile Acid binders
- MOA
- examples
- extra benefit
- block reabsorption of bile acid in liver -> contain Cl which is exchanged for bile acid in gut, and bile is excreted out through poop
- cholestipol and cholestyramine
- upreg LDL recepetor
Lipoproteins
- function
- chylomicrons: function
- VLDL: what does it have on surface; location transports, activated by, turns into
- IDL: function, turns into, how
- LDL: function, get into cell
- HDL: function,
- delivery triglycerides and cholesterol from liver to tissue
- carry lipids absorbed through GI system -> transport TG to peripheral tissue (adipose, cardiac, skeletal) and cholesterol to liver
- apoB, cholesterol, TG, apoC2 (needed for LPL) and Apo E (needed for hepatic uptake); from liver to tissues; glycoprotein lipase on endo cells -> release FFA turns into IDL
- takes triglycerides and cholesterol back to liver; hepatic lipase turns to LDL
- delivers chol to cells; endocytosis
- transports chol back to liver
Lipid Lowering Drugs
- bile acid binders
- statins
- nicotinic acid (niacin)
- fibrin acid
- fish oil
- promotes excretion of bile and liver has to make more so uses stores of chol
- HMG CoA reductase inhibitos -> doesnt allow for liver to make cholesterol
- directly decreases synthesis VLDL
- activate PPR gamma and stimulates genes for lipid metabolism
- increase TG breakdown and decrease synthesis
Familial Hypercholestolemia
- what is it
- class 1
- class 2
- class 3
- class 4
- class 5
- signs
- increased risk
- manage’
- AD, chrom 19 -> causes very high LDL levels
- LDLr absent
- LDLr not transported
- LDL cannot bind to receptor
- LDLr binds to LDL but cannot endocytose it
- LDLr not recycled
- xanthomas
- cardiovasc dx
- heterozygous can be managed with statins; homo will treat with high level of statin or statin + ezetimibe
Hyperlipidemia
- what is it
- causes
- type 1
- type 2a
- type 2b
- type 3
- type 4
- type 5
- defect in lipoprotein metabolism
- elevated TG, lipids, or both
- elevated chylomicron bc of defective lipoprotein lipase
increased LDL bc non functional receptor - over production of VLDL by liver and increased LDL bc of receptor inefficiency
- IDL elevated by lack of ApoE
- Increased VLDL bc of LPL problem
- Increased VLDL and chylomicrons bc of decrease in apo C2 (co factor for LPL)
Hypertriglyceridemia
- what is it
- sxs with severe
- caused by
- meds
- elevated TG
- lipemia retinalis and eruptive xanthomas
- lifestyle
- fibrins, statins, niacin
Jaundice
- unconj: location
- conj
- pre-hepatic (hemolysis), indirect (not water soluble, in blood but not in urine)
- intahepatic or post, direct, (water soluble, will be in urine)
Gilbert Syndrome
- what happens, when
- sxs
- UDP-glucouronyl transferase present but stops working under stress
- mild unconj bili under stress
Criggler-Najjar syndrome type 1
- what happens
- prognosis
- missing UDP glucuronyl transferase -> cant conjugate
- death in a few years
Criggler Najjar type 2
- what happens
- management
- not 2 much enzyme, conjugate some bili but not all
- phenobarbital -> increase Cl flux decreases excitability ;cyto P450 inducer
Dubin-Johson
- what happens
- deposits -> gross
- dx
- diff from rotor
- conjugates bili but cant get across canalicular membrane into duct
- in lysosome -> liver turns black from epi metabolites
- ratio of corporphyrin 3 and 1 -> usually have more 3 but will be reversed
- similar, except liver is normal colored
Cholestatic Jaundice
- caused by
- newborn
- children/ adults
- adults
- obstruction to bile flow
- choeductal cyst (cyst in common bile duct) or biliary atresia
- pancreatitis, gallstone, sclerosing cholangitis
- pancreatic CA
Halothane
- what is it
- labs
- inha;ed anesthetic that has highly fulminant hepatitis
- high AST, ALT, eosionophilia, prolonged PT thime bc clotting factors cant be made by liver
Alcohol induced fatty liver
- what is it
- epi
- stain with
- when alcohol is metabolized there is increase in NADH which shuts off TCA and stops beta oxidation leading to fat storage
- cytoplasmic vacuoles filled with fat
- sudan black or oil red
Benign Hepatic tumor
- cavernous hemangioma: epi, worried about, sxs, dx, tx
- hepatic abcess: secondary to, US shows, sxs, tx
- women on OCP; rupture with excessive bleeding; RUQ pain; US; surgery; blood filled vasc space of variable size lined by single epi layer
- bacterial infection from another place; fluid filled cavity; fever, chill RUQ pain; drain
Malignant hepatic tumor
- mcc
- hepatocellular carninoma: associated w/ caused by,
- met
- cirrhosis, hep C/B, alcoholism, wilsons dx;
Colon
- function
- ascending: pumps
- transverse
- sigmoid
- rectum
- reabsorb water
- Na/ K pumps, stimulated by aldosterone, kicks out Na and water follows; semi-solid stool
- primary (mediated by hollstra) and secondary peristalsis (based on stretch)
- stores stool
- stretch receptors activated and signals you need to go to the restroom; can contract and push back into sigmoid colon for later
Volvulus
- what is it
- sequelae
- location
- sxs
- imaging
- management
- intestine will twist upon itself on mesentary
- obstruction of GI tract or ischemia
- ileum from congenital malrotation or in sigmoid colon (redundant -> big and floppy and easy to twist)
- currant jelly stool (blood and mucus)
- x-ray will see kidney bean shaped intestine
- resection of volvulized intestine, must stay twisted to prevent re-perfusion injury
Intussusception
- what is it
- epi
- location
- sxs
- imaging
- caused by
- management
- telescoping of one segment of bowel into another
- children
- ileocecal junction
- n/v, sausage shaped mass, current jelly stool
- US, bulls eye appearance
- polyp, CA, after viral infection,
- reduce intussception and resect
Diverticulosis
- what is it
- risk factor
- caused by
- sxs
- itis: caused by, sxs, complications
- presence of diverticula in colon
- older than 60, poor diet (low fiber)
- increased intraluminal pressure + focal weakness of colonic wall
- painless bleeding
- piece of stool getting caught in outpouching -> pressure increases -> compromises blood flow; LLQ pain; perforation, peritonitis, abcess, stenosis of bowel, colovesicular fistula (pneumoturia, pass feces through urine, colonized with bugs from colon); removed diseased part of colon
Polyp
- inflammatory: caused by, histo
- hyperplastic: histo
- lymphoid: epi, histo
- hamartomas: histo, occur
- neoplastic: epi, location, types
- presentation
- UC and Crohns; composed of regenerating intestinal mucosa
- composed of well diff mucousal cells that form glands and crypts
- children, consist of intestinal mucosa infiltrates w/ lymphocytes
- mucousal glands, SM cells, CT that occurs sporadically
- seen after 55yrs, most in sigmoid/ rectum; most common is tubular, tubulovillous, and villous
- lower GI bleed, partial intestinal obstruction, large amount of mucus secretion
Familial Adenomatous Polyposis
- genetic
- what happens
- Garnder
- Turcot
- Putz-Jeghers
- Juvenile Polyposis
- AD, APC gene inheritance
- pt develops several polyps throughout colon and rectum
- polyposis, desmois tumor, osteoma of mandible/skull, sebaceous cyst
- polyposis + medulloblastoma or glioma
- AD, non-neoplastic hamartomatous polyps in stomach, intestine, colon, skin; freckling of lip
- mult polyps in GI tract of child/ young adult; > 5 polyps in colon/rectum; juvenile polyps throughout GI tract; any number of polyps w fam hx of juvenile polyposis
GI hemm
- causes of lower
- diverticulosis, angiodysplasia, UC, ischemic colitis, ulceration
- red blood in stool
Rectal bleeds
- sxs
- caused by
- red blood when wipe
- hemmorrhoids, fissures, CA, polyps
Large Intestine Obstruction
- location
- MCC
- sxs
- dx
- management
- pseudo obstruction
- sigmoid
- adenocarcinoma, scarring secondary to diverticulitis, volvulus
- n/v, crampy abd pain and distention
- distended prox colon with air fluid levels and no gas in rectum
- emergency laparatomy w/ perforation (w/ free air on diaphragm)
- look like obstruction pt but when scoped there is non; paralysis of colonc -> no peristalsis; pt on chronic opioid and anti-cholinergics; colonoscopy and decompression
Colon CA
- risks
- right sided
- left sided
- genetic, over 60, low fiber, high fat / cholesterol/ carbs, IBD
- no obstruction, iron def anemia; anorexia, malaise, and weight loss
- narrow lumen, sxs partial intestinal obstruction; changes in stool caliber, constipation, cramping abd pain, abd distention, and n/v
Lynch Syndrome
- epi
- side
- mutation
- 1
- 2
- under 50
- right
- auto dom; DNA mismatch repair (MLH1, MSH2, MSH6, PMS2)
- predisposition to colon adenocarcinoma
- predisposition to colon CA with features of lynch 1 and increased incidence of extra intestinal CA
Colon CA signs and sxs
- bowel
- weight
- bleed ->
- pain
- alternating
- weight loss
- bleeding from lower GI
- melena
- abd pain
- abd distention
- anemia, fatigue, pallor
Colon screening - no risk - w/ risk factors - dx -
- start at 50, with colonoscopy every 10 and sigmoid every 5 yrs
- start at 40 yrs old or 10 yrs before onset of family member affected
- biopsy
hemmorhoids
- internal
- external
- caused by
- degree
- dx
- tx
- above dentate line, not painful -> viscerally innervated
- below dentate line, painful -> somatic innervation
- congestion of veins in hemorrhoidal plexus, bc of constipation and increase in pressure squeezing and not allowing drainage
- 1: no prolapse, 2: prolapse with defecation then returns on own, 3: prolapse with defecation that requires manual reduction, 4: always prolapsed, unable to be reducible manually
- DRE
- increase fiber, drink more water, use sitz bath (pt sits in warm water 3x a day and after bowel movement, keeps area clean), proctocream (lidocaine mixed with steroids (numbs and decreases inflammation); internal is removed surgically
anal fistula
- what is it
- result of
- patho
- sequelae
- management
- connection between rectum and perianal skin
- anal crypt infection
- anal crypt becomes infected and an abcess forms and ruptures forming connection between anus and perianal skin
- perianal skin scars down, then ruptures, drains (intermittent purulent discharge)
- can erode into
- remove tunnel and allow it to fill in
Anal fissure
- what is it
- location
- caused by
- sequelae
- sxs
- tx
- longitudinal tear in anal mucosa
- posterior midline, near anal verge
- irritation and breakage of canals epi; diarrhea, constipation, excessie anal tension or trauma
- spasm of internal anal sphincter which is painful
- tearing pain + bright red blood per rectum (drops of blood into toilet water or when wiping)
- anoscopy
- stool softener, increase fluids, avoid constipating foods, add fiber, sitz bath
CA of rectum
- type
- epi
- sxs
- dx
- tx
- lymph invovlement
- adeno
- female
- rectal bleeding, alt bowel habits, obstruction, tenesmus (feeling you have to defecate but dont)
- colonoscopy
- surgery -> save anal sphincter
- add radiation and 5 FU
CA of anus
- type
- risks
- sxs
- managment
- squamous cell
- crohns, fistula, abcess, infection
- mucus evacuation with feces
- chemo and radiation -> shrink -> then excise
Appendix
- what is it
- itis patho
- mcburneys point
- sxs
- sign
- managment
- appendage attached to base of cecum
- inflammation caused by piece of stool obstucting opening -> continues to produce mucus -> increase in pressure -> becomes edematous and activates visceral pain receptors (non specific peri-umbilical pain -> compromised blood flow -> ischemic / necrotic (somatic innervation impacted and pain localizes at mcburneys point)
- 2/3 away from umbilicus towards ASIS
- n/v, diarrhea, fever, annorexia
- psoas sign (straight leg illicits RLQ pain), obturator sign flex at hip and knee, internal rotate with pain in RLQ, rothburg - palpate LLQ and feel pain in RLQ
- NPO, NG tube, IV NS, Meperidine, appendectomy
Crohns
- epi
- starts as
- whats involved
- starts with
- protein involved
- normal immune response is
- pathogenesis
- extra intestinal mainfestations
- 20-30 yrs
- abd pain, diarrhea, weight loss, low grade fever, aphthuous ulcer of oral mucosa
- entire GI wall is inflammed
- terminal illetus
- NK-kappaB increased activity
- blunted, microbes persist, induce chronic inflamm
- increased activity of Th1 helper cells -> increase production of IL-2, INF gamma, and TNF -> ganulomas
- erythema nodusum, arthritis, ankylosing spondylitis, fistulas, strictures, abcesses, peri-anal dx
- non-caseating granuloma and cobblestone appearance -> long linear ulcers
Ulcerative Colitis
- hallmark finding
- whats involved
- histo
- complication
- bloody diarrhea w or w/o abd pain
- rectum and large intestine only
- continuous damage
- ## toxic megacolon (dilation in transverse colon) -> surgery and antibiotics
C diff
- gram
- respiration
- forms
- causes
- sxs
- how to avoid
- prevent with
- dx
- tx
- +
- anaerobe
- spore forming
- anti-biotic pseudomembranous colitis
- toxin causes diarrhea, bloating abd pain
- wash hands
- cytotoxic assay, stool leukocyte measurements
- metro and vanco
Derm Herpetiformis
- sxs
- distribution
- type
- histo
- sxs
- group of small vessicles that occur on extensor surfaces
- symmetric
- AI
- PMN and fibrin at tips of dermal papillae
- diarrhea, steatorrhea, other malabsorption
Tropical Sprue
- what is it
- infection
- sxs
- causes
- malabsorption dx commonly found in tropical region
- infection of flat villi
- diarrhea/ steatorrhea, fever, malaise
- fat soluble deficiency, vit b 12 deficiency
Lactose Intolerance
- primary
- secondary
- normally
- sxs
- genetic, asian and african
- MC a response to intestinal mucousal dx
- degenerates with age
- GI upset upon ingestion of food with lactose
Necrotizing Enterocolitis
- what happens
- epi
- caused by
- imaging
- patho finding
- gas bowel; how
- portions of bowel undergo necrosis
- premature infants
- lack pf developed blood vessels
- fixed loop, w/ unilateral gas-filled loop of bowel
- pneumatosis intestinalis -> gas within wall of small intestine -> look like gas cyst; air is produced by bacteria residing in bowel wall
IBS
- epi
- triggers
- sxs
- dx
- managment
- females, 20’s
- stress/ anxiety related
- constipation/ diarrhea
- exclusion
- fiber supplements
Whipple Dx
- what is it
- caused by
- epi
- sxs
- other damage
- dx
- tx
- small intestines cannot absorb nutrients
- tropheryma whipplei
- middle age males
- joint pain
- heart, brain
- small bowerl biopsy -> + for periodic acid schiff staining
- cephalosporin
Whipple Dx
- what is it
- caused by
- epi
- sxs
- other damage
- dx
- tx
- small intestines cannot absorb nutrients
- tropheryma whipplei
- middle age males
- joint pain
- heart, brain
- small bowerl biopsy -> + for periodic acid schiff staining
- cephalosporin followed w/ one year TMP-sulfa